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Article ; Online: Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury.

Buse, Marc / Cheng, Mingbo / Jankowski, Vera / Lellig, Michaela / Sterzer, Viktor / Strieder, Thiago / Leuchtle, Katja / Martin, Ina V / Seikrit, Claudia / Brinkkoettter, Paul / Crispatzu, Giuliano / Floege, Jürgen / Boor, Peter / Speer, Timotheus / Kramann, Rafael / Ostendorf, Tammo / Moeller, Marcus J / Costa, Ivan G / Stamellou, Eleni

iScience

2024 Volume 27, Issue 3, Page(s) 109255

Abstract: Tubular injury is the hallmark of acute kidney injury (AKI) with a tremendous impact on patients and health-care systems. During injury, any differentiated proximal tubular cell (PT) may transition into a specific injured phenotype, so-called "scattered ... ...

Abstract	Tubular injury is the hallmark of acute kidney injury (AKI) with a tremendous impact on patients and health-care systems. During injury, any differentiated proximal tubular cell (PT) may transition into a specific injured phenotype, so-called "scattered tubular cell" (STC)-phenotype. To understand the fate of this specific phenotype, we generated transgenic mice allowing inducible, reversible, and irreversible tagging of these cells in a murine AKI model, the unilateral ischemia-reperfusion injury (IRI). For lineage tracing, we analyzed the kidneys using single-cell profiling during disease development at various time points. Labeled cells, which we defined by established endogenous markers, already appeared 8 h after injury and showed a distinct expression set of genes. We show that STCs re-differentiate back into fully differentiated PTs upon the resolution of the injury. In summary, we show the dynamics of the phenotypic transition of PTs during injury, revealing a reversible transcriptional program as an adaptive response during disease.
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109255
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Article ; Online: Effect of glucocorticoid treatment on BAFF and APRIL expression in patients with immune thrombocytopenia (ITP).

Kamhieh-Milz, Julian / Ghosoun, Nuha / Sterzer, Viktor / Salama, Abdulgabar

Clinical immunology (Orlando, Fla.)

2017 Volume 188, Page(s) 74–80

Abstract: Immune thrombocytopenic purpura (ITP) is an idiopathic bleeding disorder. B cell activating factor (BAFF) and 'A proliferation-inducing ligand' (APRIL) have regulatory effects on B and T cells and may represent relevant factors in the pathogenesis of ITP. ...

Abstract	Immune thrombocytopenic purpura (ITP) is an idiopathic bleeding disorder. B cell activating factor (BAFF) and 'A proliferation-inducing ligand' (APRIL) have regulatory effects on B and T cells and may represent relevant factors in the pathogenesis of ITP. Serum levels and gene expression were investigated in ITP patients. Both BAFF and APRIL serum levels were significantly elevated in active ITP. However, gene expression analysis revealed both factors to have a tendency toward downregulation. Glucocorticoid treatment significantly reduced BAFF but not APRIL serum levels, which may be mediated by differences in transcription factor binding sites. The glucocorticoid receptor binding site is present in the BAFF promotor region, but not in the APRIL promotor region. Prednisolone in combination with vitamin D3 may be effective in reducing APRIL serum levels. In conclusion, glucocorticoid treatment exerts different regulatory effects on both BAFF and APRIL, whereas antioxidant supplementation may also be beneficial in reducing serum levels.
MeSH term(s)	Adult ; Aged ; B-Cell Activating Factor/blood ; B-Cell Activating Factor/genetics ; B-Cell Activating Factor/metabolism ; Binding Sites/genetics ; Cholecalciferol/therapeutic use ; Drug Therapy, Combination ; Female ; Gene Expression Regulation/drug effects ; Glucocorticoids/therapeutic use ; Humans ; Male ; Middle Aged ; Prednisolone/therapeutic use ; Promoter Regions, Genetic/genetics ; Purpura, Thrombocytopenic, Idiopathic/drug therapy ; Purpura, Thrombocytopenic, Idiopathic/genetics ; Purpura, Thrombocytopenic, Idiopathic/metabolism ; Receptors, Glucocorticoid/metabolism ; Tumor Necrosis Factor Ligand Superfamily Member 13/blood ; Tumor Necrosis Factor Ligand Superfamily Member 13/genetics ; Tumor Necrosis Factor Ligand Superfamily Member 13/metabolism ; Vitamins/therapeutic use
Chemical Substances	B-Cell Activating Factor ; Glucocorticoids ; Receptors, Glucocorticoid ; TNFSF13B protein, human ; Tumor Necrosis Factor Ligand Superfamily Member 13 ; Vitamins ; Cholecalciferol (1C6V77QF41) ; Prednisolone (9PHQ9Y1OLM)
Language	English
Publishing date	2017-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2017.12.010
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Zs.A 880: Show issues

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Article ; Online: CCR1 and CCR2 antagonists.

Zimmermann, Henning W / Sterzer, Viktor / Sahin, Hacer

Current topics in medicinal chemistry

2014 Volume 14, Issue 13, Page(s) 1539–1552

Abstract: Chemokines constitute a family of small heparin-binding proteins which orchestrate the infiltration of leukocytes during inflammation, but also directly influence other physiological and pathophysiological processes. In humans, more than 40 chemokines ... ...

Abstract	Chemokines constitute a family of small heparin-binding proteins which orchestrate the infiltration of leukocytes during inflammation, but also directly influence other physiological and pathophysiological processes. In humans, more than 40 chemokines are known binding to around 18 G-protein-coupled receptors. A non-redundant role of certain chemokines and their receptors has been identified within the last years in inflammation and host defense. Among chemokine receptors, the CC chemokine receptors CCR1 and CCR2 have been shown to play a crucial role in these processes. Importantly, these receptors have already been targeted by specific antagonists in early human trials for autoimmune and infectious diseases. Although most of these antagonists failed to show any significant efficacy in the clinic, the knowledge of their biological effects could henceforth offer new avenues with optimal strategies for producing successful therapeutics.
MeSH term(s)	Humans ; Molecular Structure ; Receptors, CCR1/antagonists & inhibitors ; Receptors, CCR1/immunology ; Receptors, CCR1/metabolism ; Receptors, CCR2/antagonists & inhibitors ; Receptors, CCR2/immunology ; Receptors, CCR2/metabolism ; Small Molecule Libraries/chemistry ; Small Molecule Libraries/pharmacology ; Structure-Activity Relationship
Chemical Substances	Receptors, CCR1 ; Receptors, CCR2 ; Small Molecule Libraries
Language	English
Publishing date	2014-08-19
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064823-6
ISSN	1873-4294 ; 1568-0266
ISSN (online)	1873-4294
ISSN	1568-0266
DOI	10.2174/1568026614666140827144115
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Zs.A 5572: Show issues

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Article ; Online: Effects of Perfusion Pressures on Podocyte Loss in the Isolated Perfused Mouse Kidney.

Strieder, Thiago / Puelles, Victor G / Vogt, Michael / Buhl, Eva M / Saritas, Turgay / Hausmann, Ralf / Sterzer, Viktor / Leuchtle, Katja / Boor, Peter / Floege, Jürgen / Moeller, Marcus J / Stamellou, Eleni

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2021 Volume 55, Issue S4, Page(s) 1–12

Abstract: Background/aims: Podocytes are lost in most glomerular diseases, leading to glomerulosclerosis and progressive kidney disease. It is generally assumed, that podocytes are exposed to the filtration flow and thus to significant shear forces driving their ... ...

Abstract	Background/aims: Podocytes are lost in most glomerular diseases, leading to glomerulosclerosis and progressive kidney disease. It is generally assumed, that podocytes are exposed to the filtration flow and thus to significant shear forces driving their detachment from the glomerular basement membrane (GBM). In this context, foot process effacement has been proposed as potential adaptive response to increase adhesion of podocytes to the GBM. Methods: We have tested these hypotheses using optical clearing and high-resolution 3-dimensional morphometric analysis in the isolated perfused murine kidney. We investigated the dynamics of podocyte detachment at different perfusion pressures (50, 300 and more than 450 mmHg) in healthy young or old mice (20 vs. 71 weeks of age), or mice injected with anti-GBM serum to induce global foot process effacement. Results: Results show that healthy podocytes in young mice are tightly attached onto the GBM and even supramaximal pressures did not cause significant detachment. Compared to young mice, in aged mice and mice with anti-GBM nephritis and foot process effacement, gradual progressive loss of podocytes had occurred already before perfusion. High perfusion pressures resulted in a relatively minor additional loss of podocytes in aged mice. In mice with anti-GBM nephritis significant additional podocyte loss occurred at this early time point when increasing perfusion pressures to 300 mmHg or higher. Conclusion: This work provides the first experimental evidence that podocytes are extraordinarily resistant to acutely increased perfusion pressures in an ex vivo isolated kidney perfusion model. Only in glomerular disease, significant numbers of injured podocytes detached following acute increases in perfusion pressure.
MeSH term(s)	Aging ; Animals ; Cell Adhesion ; Cell Survival ; Female ; Glomerular Basement Membrane/cytology ; Glomerular Basement Membrane/pathology ; Kidney Diseases/pathology ; Male ; Mice ; Perfusion ; Podocytes/cytology ; Podocytes/pathology ; Pressure
Language	English
Publishing date	2021-04-13
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.33594/000000355
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Zs.A 3160: Show issues

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Article ; Online: Expression of the Metalloproteinase ADAM8 Is Upregulated in Liver Inflammation Models and Enhances Cytokine Release

Awan, Tanzeela / Babendreyer, Aaron / Wozniak, Justyna / Alvi, Abid Mahmood / Sterzer, Viktor / Cook, Lena / Bartsch, Jörg W / Liedtke, Christian / Yildiz, Daniela / Ludwig, Andreas

Mediators of inflammation

2021 Volume 2021, Page(s) 6665028

Abstract: Acute and chronic liver inflammation is driven by cytokine and chemokine release from various cell types in the liver. Here, we report that the induction of inflammatory mediators is associated with a yet undescribed upregulation of the metalloproteinase ...

Abstract	Acute and chronic liver inflammation is driven by cytokine and chemokine release from various cell types in the liver. Here, we report that the induction of inflammatory mediators is associated with a yet undescribed upregulation of the metalloproteinase ADAM8 in different murine hepatitis models. We further show the importance of ADAM8 expression for the production of inflammatory mediators in cultured liver cells. As a model of acute inflammation, we investigated liver tissue from lipopolysaccharide- (LPS-) treated mice in which ADAM8 expression was markedly upregulated compared to control mice.
MeSH term(s)	ADAM Proteins/genetics ; ADAM Proteins/metabolism ; Animals ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Cytokines/metabolism ; Hepatitis/metabolism ; Inflammation/metabolism ; Kupffer Cells/metabolism ; Lipopolysaccharides/metabolism ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Antigens, CD ; Cytokines ; Lipopolysaccharides ; Membrane Proteins ; Tumor Necrosis Factor-alpha ; ADAM Proteins (EC 3.4.24.-) ; Adam8 protein, mouse (EC 3.4.24.-)
Language	English
Publishing date	2021-03-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2021/6665028
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Zs.A 3575: Show issues

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Book ; Online ; Thesis: Der Einfluss von Endoglin auf die Fibrose, sowie die Inflammation und Regeneration in der Leber

Sterzer, Viktor [Verfasser] / Schirawski, Jan [Akademischer Betreuer] / Ludwig, Andreas [Akademischer Betreuer]

2017

Author's details	Viktor Sterzer ; Jan Schirawski, Andreas Ludwig
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	German
Publisher	Universitätsbibliothek der RWTH Aachen
Publishing place	Aachen
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Identification of novel autoantigens via mass spectroscopy-based antibody-mediated identification of autoantigens (MS-AMIDA) using immune thrombocytopenic purpura (ITP) as a model disease.

Kamhieh-Milz, Julian / Sterzer, Viktor / Celik, Hatice / Khorramshahi, Omid / Fadl Hassan Moftah, Reham / Salama, Abdulgabar

Journal of proteomics

2017 Volume 157, Page(s) 59–70

Abstract: Immune thrombocytopenic purpura (ITP) is one of the best characterized autoimmune diseases. Autoantibodies (AABs) against platelet antigens are considered as the diagnostic hallmark of ITP, but are detectable in only 50% of patients. We designed and ... ...

Abstract	Immune thrombocytopenic purpura (ITP) is one of the best characterized autoimmune diseases. Autoantibodies (AABs) against platelet antigens are considered as the diagnostic hallmark of ITP, but are detectable in only 50% of patients. We designed and applied a novel proteomic approach termed Mass Spectroscopy-based Antibody-Mediated Identification of Autoantigens (MS-AMIDA) for platelet antigens. Patients were separated into patients with classical AABs [ITP(+)] and patients without AABs [ITP(-)]. Altogether, 181 potential AAGs were found in ITP(+) and 135 AAGs in ITP(-), with 34 and 23 AAGs reproducibly found in two runs of MS-AMIDA. After subtracting identifiers from the controls, 57 AAGs in ITP(+) and 29 AAGs in ITP(+) remained, with 16 AAGs commonly found in ITP(+) and ITP(-) patients. Label-free quantification (LFQ) revealed 15 potential AAGs that are quantitatively stronger in ITP. Dot blot validation was performed on hexokinase 1 (HK1), E1 pyruvate dehydrogenase (E1-PDH), coagulation factor XIII, filamin A (FLNA), non-muscle myosin 9. Eleven patients were found to have anti-HK1 AABs, one patient had anti-E1-PDH AABs, and two patients had anti-FLNA AABs. Most antigens were of intracellular origin with significant association with actin-cytoskeleton and regulation of programmed cell death. In conclusion, novel AAGs for ITP were identified using MS-AMIDA.
Language	English
Publishing date	2017-03-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2017.01.012
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Article ; Online: Reduced antioxidant capacities in platelets from patients with autoimmune thrombocytopenia purpura (ITP).

Kamhieh-Milz, Julian / Bal, Gürkan / Sterzer, Viktor / Kamhieh-Milz, Sundrela / Arbach, Olga / Salama, Abdulgabar

Platelets

2012 Volume 23, Issue 3, Page(s) 184–194

Abstract: Autoimmune thrombocytopenic purpura (ITP) is characterized by an abnormally low platelet count and bleeding risks. The exact triggering event remains elusive. Oxidative stress may play a role in several autoimmune diseases. A direct link between ... ...

Abstract	Autoimmune thrombocytopenic purpura (ITP) is characterized by an abnormally low platelet count and bleeding risks. The exact triggering event remains elusive. Oxidative stress may play a role in several autoimmune diseases. A direct link between platelets in ITP and oxidative stress has not yet been addressed. The intracellular platelet antioxidant capacity (AOC) in ITP patients in the active phase (n = 24) and remission (n = 12), and 44 healthy controls were analysed with 2',7'-dichlorodihydrofluorescein diacetate, and in combination with hydrogen peroxide. Enzyme activities (EA) of serum glutathione peroxidase (GPx), glutathione reductase (GRed) and catalase (CAT) were investigated colourimetrically in patients and controls. The AOC of ITP patients in the active phase was drastically reduced, with significantly high mean fluorescence intensity values. Higher GPx activity was observed in both active phase and remission in comparison to healthy controls (p < 0.001), with greater activity observed in active ITP than remission (p = 0.001). However, GRed EA was not elevated indicating that reduced glutathione (GSH) is not comparably recovered as consumed, leading to a decreased bioavailability of GSH and increased oxidative stress. These results suggest that oxidative stress is implicated in active ITP and may play a crucial role in its pathophysiology.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Antioxidants/metabolism ; Blood Platelets/metabolism ; Female ; Fluoresceins/chemistry ; Hemorrhage/blood ; Hemorrhage/etiology ; Hemorrhage/therapy ; Humans ; Hydrogen Peroxide/chemistry ; Male ; Middle Aged ; Oxidative Stress ; Oxidoreductases/blood ; Platelet Count ; Purpura, Thrombocytopenic, Idiopathic/blood ; Purpura, Thrombocytopenic, Idiopathic/complications ; Purpura, Thrombocytopenic, Idiopathic/therapy
Chemical Substances	2',7'-dichlorodihydrofluorescein diacetate ; Antioxidants ; Fluoresceins ; Hydrogen Peroxide (BBX060AN9V) ; Oxidoreductases (EC 1.-)
Language	English
Publishing date	2012
Publishing country	England
Document type	Clinical Trial ; Journal Article
ZDB-ID	1034283-7
ISSN	1369-1635 ; 0953-7104
ISSN (online)	1369-1635
ISSN	0953-7104
DOI	10.3109/09537104.2011.610909
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Zs.A 2888: Show issues

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Article ; Online: Secretome profiling of apheresis platelet supernatants during routine storage via antibody-based microarray.

Kamhieh-Milz, Julian / Mustafa, Shakhawan A / Sterzer, Viktor / Celik, Hatice / Keski, Sahime / Khorramshahi, Omid / Movassaghi, Kamran / Hoheisel, Jörg D / Alhamdani, Mohamed S S / Salama, Abdulgabar

Journal of proteomics

2017 Volume 150, Page(s) 74–85

Abstract: Platelet storage lesions (PSLs) occur during platelet concentrate (PC) storage. Adverse transfusion reactions (ATRs) have been demonstrated to be more frequent in older PCs and removal of the supernatant prior to transfusion reduces their occurrence. ... ...

Abstract	Platelet storage lesions (PSLs) occur during platelet concentrate (PC) storage. Adverse transfusion reactions (ATRs) have been demonstrated to be more frequent in older PCs and removal of the supernatant prior to transfusion reduces their occurrence. Proteomic profiling of PC supernatants was thus performed to identify proteins associated with PSLs and ATRs. Twenty-four PCs were investigated daily from day 0 to day 9 for platelet pre-activation (PPA), platelet-derived extracellular vesicles (PEVs), and platelet function. Using antibody microarrays, 673 extracellular proteins were analysed in PC supernatants on days 0, 3, 5, 7, and 9. During 5days of storage, PPA and PEVs continuously increased (P<0.0001). Platelet function was observed to remain stable within the first 5days (P=0.1751) and decreased thereafter. Comparison of all time points to day 0 revealed the identification of 136 proteins that were significantly changed in abundance during storage, of which 72 were expressed by platelets. Network analysis identified these proteins to be predominantly associated with exosomes (P=4.61×10 Significance: Changes in platelet concentrate (PC) supernatants during storage have been so far only poorly addressed and high abundant proteins burden the identification of quantitative changes in the secretome. We applied a high-throughput antibody microarray allowing for the sensitive quantification of 673 extracellular factors. PCs account for the highest number of adverse transfusion reactions (ATRs). ATRs have been demonstrated to be more frequent in older PCs and removal of the supernatant prior to transfusion reduces their occurrence. Comprehensive interpretation of the changing proteins in the secretome during platelet storage under blood banking conditions may help to identify mechanisms leading to the occurrence of adverse transfusion reactions.
Language	English
Publishing date	2017-01-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2016.07.028
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Article ; Online: Endoglin in human liver disease and murine models of liver fibrosis-A protective factor against liver fibrosis.

Alsamman, Muhammad / Sterzer, Viktor / Meurer, Steffen K / Sahin, Hacer / Schaeper, Ute / Kuscuoglu, Deniz / Strnad, Pavel / Weiskirchen, Ralf / Trautwein, Christian / Scholten, David

Liver international : official journal of the International Association for the Study of the Liver

2017 Volume 38, Issue 5, Page(s) 858–867

Abstract: Background & aims: Liver fibrosis is the outcome of chronic liver injury. Transforming growth factor-β (TGF-β) is a major profibrogenic cytokine modulating hepatic stellate cell (HSC) activation and extracellular matrix homeostasis. This study analyses ... ...

Abstract	Background & aims: Liver fibrosis is the outcome of chronic liver injury. Transforming growth factor-β (TGF-β) is a major profibrogenic cytokine modulating hepatic stellate cell (HSC) activation and extracellular matrix homeostasis. This study analyses the effect of Endoglin (Eng), a TGF-β type III auxiliary receptor, on fibrogenesis in two models of liver injury by HSC-specific endoglin deletion. Methods: Eng expression was measured in human and murine samples of liver injury. After generating GFAP Results: Endoglin is upregulated in human liver injury. The receptor is expressed in liver tissues and mesenchymal liver cells with much higher abundance of the L-Eng splice variant. Comparing GFAP Conclusion: Endoglin isoforms are differentially upregulated in liver samples of patients with chronic and acute liver injury. Endoglin deficiency in HSC significantly aggravates fibrosis in response to injury in two different murine models of liver fibrosis and increases α-SMA and fibronectin expression in vitro. This suggests that Endoglin protects against fibrotic injury, likely through modulation of TGF-β signalling.
MeSH term(s)	Animals ; Disease Models, Animal ; Endoglin/genetics ; Endoglin/metabolism ; Fibronectins/metabolism ; Hepatic Stellate Cells/metabolism ; Humans ; Liver/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protective Factors ; Signal Transduction ; Transforming Growth Factor beta/metabolism
Chemical Substances	ENG protein, human ; Endoglin ; Eng protein, mouse ; Fibronectins ; Transforming Growth Factor beta
Language	English
Publishing date	2017-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.13595
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